Mapping the peripheral sensory dimension of dystonia: a five-axis analysis.

Dystonia is conventionally attributed to dysfunction in central motor circuits, yet several clinical features, including sensory tricks, task specificity, and abnormalities in somatosensory processing, indicate an influence of sensory input. Whether peripheral sensory afferents are passive conduits to central circuits or contribute to dystonia pathophysiology remains unresolved. To examine whether peripheral sensory afferents participate in dystonia networks beyond their role as upstream inputs. Evidence was synthesized across five domains: phenomenology, electrophysiology, neuroimaging, genetics, and treatment. Priority was given to studies that manipulated or quantified peripheral afferent input and assessed effects on motor output or network physiology. Sensory tricks produce rapid improvement across dystonia phenotypes, indicating that afferent input can influence motor output. Electrophysiological studies demonstrate impaired afferent modulation of intracortical inhibition, abnormal integration of converging sensory inputs, and reduced reflex suppression at spinal and brainstem levels. Neuroimaging studies show somatosensory representations and changes in network activity. Genetic and animal studies implicate dystonia-associated pathways in the regulation of proprioceptive afferent signaling, and sensory-neuron-specific manipulations can induce or reduce abnormal movements. Therapeutic interventions, including peripheral stimulation, botulinum toxin, and sensory blockade, have been associated with reductions in dystonic symptoms through mechanisms that alter afferent input. Findings from phenomenological, electrophysiological, neuroimaging, genetic, and therapeutic studies indicate that peripheral sensory afferents contribute to dystonia networks. These observations are consistent with a model in which abnormalities of afferent gating, sensory integration, and somatosensory representation contribute to dystonic expression across multiple levels of the neuraxis, with potential implications for therapeutic targeting.